Some Observations on the Role of the Lymphatics in Experimental Acute Pulmonary Edema

Abstract

Lymph was collected from the right duct and thoracic duct of 13 dogs in which acute pulmonary edema was produced by partial obstruction of the left atrium by means of a balloon. Elevation of left atrial pressure to 30 mm. Hg resulted in an increase in thoracic duct flow within 30 minutes, followed by an increase in right duct flow within the next 15 minutes. Critical pulmonary edema became manifest approximately 30 minutes after the onset of increased right duct flow, and the dogs died in pulmonary edema approximately 90 minutes after inflation of the left atrial balloon, unless the left atrial pressure was reduced. The per cent of fluid in serial lung biopsies increased in the first biopsy taken 15 minutes after the elevation of left atrial pressure to 30 mm. Hg, and the increase was sustained, resulting in engorgement of the lungs unless the left atrial pressure was decreased. The small absolute increase in lymph from the right duct suggests that the lymphatics are unable to function significantly to relieve the pulmonary edema produced in the.se acute experiments, resulting in an overflow of fluid into the tracheobronchial tree. C41utamic oxalacetic transaminase showed marked increases in the lymph from the right duct but only modest increases in the lymph from the thoracic duct throughout the experiments. Pyruvic transaminase in lymph from the right and thoracic ducts was relatively unchanged.

Responses of slowly and rapidly adapting receptors in the airways of rabbits to changes in the Starling forces.

“…A vascularly isolated pouch (length approximately 3 cm) was created in the right external jugular vein by occluding the veins surrounding the point(s) of entry of the lymphatic ducts in the manner described by Uhley, Leeds, Sampson & Friedman (1961) and Ravi et al (1988 (Snedecor & Cochran, 1980). In protocol 2, the stimulus-response curves before and after plasmapheresis were compared using an analysis of covariance.…”

“…Thus, by creating a similar pouch near the points of entry of the right lymphatic ducts into the right external jugular vein and increasing the pressure within it, it was possible to obstruct the flow of lymph from the lung. A pressure of 30 cmH2O was selected because it has been reported that the 'pumping pressure' in the lymphatic vessels close to the external jugular vein is approximately 17 cmH2O (Uhley et al 1961). It was found that activity of RAR increased progressively from the first minute after lymphatic obstruction.…”

Contribution of systemic venous hypertension to the development of pulmonary edema in dogs.

“…Stop-flow techniques suggest about 10 cm H 2 O, 13 whereas elevated catheter methods suggest about 17 cm lymph. 14 Either would have been exceeded by the level of systemic venous hypertension in our experiments and often observed in patients. Pang et al 15 were unable to demonstrate differences in lung fluid accumulation between systemic venous pressures of 10 and 25 mm Hg.…”

The relationship between right duct lymph flow and extravascular lung water in dogs given alpha-naphthylthiourea.

“…The development of ANTU-induced pulmonary edema did not affect this ratio despite significant increases in lymph flow. On the other hand, augmenting right duct lymph flow by producing pulmonary venous hypertension is associated with reductions in right duct lymph protein concentration (2,12,32). Since no decrease in the ratio of lymph to plasma protein concentrations was observed in ANTU-induced edema, some increase in pulmonary capillary permeability probably occurred.…”

“…The lung has an extensive lymphatic network and, in the 30 years since the pioneering work of Warren and Drinker (2), the flow and composition of pulmonary lymph have been described in normal dogs and in dogs with various conditions associated with increased extravascular lung water (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16). However, the factors which govern pulmonary lymph drainage are not fully understood.…”